1) Anaemia is common in chronic kidney disease (CKD) due to reduced kidney function and erythropoietin production. It can cause lower quality of life and increased risk of cardiovascular complications.
2) Guidelines recommend diagnosing anaemia of CKD in adults with estimated glomerular filtration rate (eGFR) <60 mL/min/1.73m2 and hemoglobin ≤11 g/dL.
3) Treatment involves iron supplementation and erythropoiesis-stimulating agents (ESAs) to increase hemoglobin levels, with a target range of 11-12 g/dL according to recent guidelines. Higher targets may increase risk without clear benefits.
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Anaemia of chronic kidney disease GUIDELINES TO PRACTICE 2013
1. Anaemia of chronic kidney
disease
“GUIDELINES TO PRACTICE ”
Dr Ayman SEDDIK , Msc , MD
ASS. PROF. NEPHROLOGY, AIN SHAMS UNIVERSITY
CONSULTANT NEPHROLOGIST DUBAI HEALTH
AUTHORITY
2. objectives
ANAEMIA OF CKD CAUSES & CONSEQUENCES
K-DIGO GUIDELINES 2012 , Eurpean best practice
guidelines statement 2013 , data from DOPS 2013
I) Diagnosis and evaluation of anemia in CKD
2) Use of iron
3) Use of Erythrocyte stimulating agents ESAs and other
agents
4) evaluation and correction of persistent failure to reach or
maintain intended haemoglobin concentration
5) evaluation of pure red blood cell aplasia
6) Red cell transfusion to treat anemia in CKD
11. Anemia is a condition in which the number of
RBCs or their oxygen-carrying capacity is
insufficient to meet physiologic needs, which
vary by age, sex, altitude, smoking, and
pregnancy status (WHO).
For diagnosis and further evaluation Hb values
according to NKF guidelines:
• <13.5 g/dL in adult males. (WHO-13g/dL)
• <12.0 g/dL in adult females.
13. QUALITY OF LIFE:
Anemia results in poorer quality of life in patients with renal
failure.
This correlation can be proven by the poor quality of life scores
in patients with lower Hb values.
Many observational as well as RCT have positively
demonstrated that the QOL scores improved in patients who
were given ESA and iron to increase their Hb
14. Generation of hypoxia due to anemia is poorly
tolerated in patients with preexisting cardiac and
vascular diseases. Compensatory mechanisms leads
to development of LVH.
Observational studies do show an increase in
mortality in patients with CKD but not direct
casualty.
Interventional studies (DOPPS) show that for an
increase of 1g/dL of Hb results in 4% decline in
mortality.
Also, Medicare data show that CKD=100% and
15. CV disease related mortality is 15 times more in
patients with CKD.
50% of deaths in patients with CKD are due to
CV disease.
LVH is the most common abnormality seen in
patients with CKD and there is a strong
correlation between anemia and LVH.
Tissue hypoxia due to anemia is the principal
stimuli triggering the compensatory changes that
stresses the CV system
16. Acceleration of progression of kidney disease by
oxygen deprivation.
Increased risk of bacteremia (11% increased risk
for every 1g/dl fall in Hb)
Detrimental effects on brain and cognitive
functions.
20. rHuEPO was genetically modified proteins that
were very similar to the nascent EPO.
Contained the 165AA backbone with one O-
linked and three N-linked gycosylated chains.
There gycosailylated chains contain variable
amounts of sialic acid residues.
Many forms of rHuEPO are available: Alfa,
21. Methoxy polyethylene glycol-epoetin beta is
made from erythropoietin by chemically linking
the N-terminal amino group or the Є-amino
group of any lysine present in the protein with
methoxy polyethylene glycol butanoic acid.
The average molecular weight is approximately
60kDa
Marketed as Mircera (Roche)
27. The use of darbepoetin alfa (to achieve a higher Hb
target) in patients with diabetes, chronic kidney disease,
and moderate anemia who were not undergoing dialysis
did not reduce the risk of either of the two primary
composite outcomes (either death or a cardiovascular
event or death or a renal event) and was associated with
an increased risk of stroke.
This risk may outweigh the potential benefits.
28. Anemia is a significant contributor to mortality
and morbidity in CKD.
ESA and iron supplementation forms the core of
anemia management and has to be understood in
detail.
The data on the upper limit of target Hb is
conflicting but there is a trend towards a lower
value.
29. Diagnosis of anaemia of CKD in adults
eGFR < 60ml/min/1.73m2
AND Hb ≤ 11 g/dl
No
Consider
other causes
Yes
Non renal and
haematinic
deficiency excluded?
No
Treat and repeat
Hb
Yes
Patient on
haemodialysis?
No
See sections
1.2 & 1.3
Yes
See initial
management
algorithm
30. Hb maintenance algorithm
(assumes ESA therapy and maintenance i.v. iron)
Measure Hb
Hb < 11 g/dl Hb 11–12 g/dl Hb 12–15 g/dl Hb > 15 g/dl
↑ ESA dose/
frequency as
per schedule
unless Hb
rising by
1/g/dl/month.
Check Hb
as per
Schedule.
No change
unless Hb
rising by
1g/dl/month
in which case
consider
ESA dose
adjustment
Consider
stopping i.v.
iron. ↓ ESA
dose/frequency
as per schedule
unless Hb
falling by more
than 1g/dl/month.
Check Hb as
per schedule.
Stop i.v. iron.
Consider
stopping
ESA or halve
dose/frequency.
Check Hb in
2 weeks.
If Hb is
persistently low
see poor
response
algorithm
Ferritin < 200 µg/l?